Anesthetic Considerations in the Acutely Injured Patient
Few situations are more challenging than the management of the acutely traumatized patient. It is the leading cause of death in individuals younger than 45 years.1,2 Up to 75% of these deaths occur within hours of injury. Effective management requires cooperation and communication between a team of physicians.
Physical Examination
Injuries Affecting the Airway
The initial examination may be limited. Injuries may be missed during the primary assessment, both in the emergency department and operating room. Undiagnosed cervical spine injuries, pneumothorax, or thoracoabdominal vascular injuries may cause significant intraoperative or postoperative morbidity or mortality. A secondary assessment or reexamination of the patient, including a review of the radiographs and laboratory results before surgery if the patient is not immediately operated on, or postoperatively, has been shown to diagnose 90% of significant injuries missed during the initial examination.3
Maxillofacial Injury
Le Fort fractures produce a disruption of the pterygoid plates that may result in the posterior displacement of the maxilla. At the Le Fort I level, this may result in an anterior open bite but generally does not produce airway obstruction secondary to the skeletal displacement. The severity of the open bite, however, may cause difficulty in achieving a satisfactory mask fit. Posterior and downward displacement of a Le Fort III fracture may result in obstruction of the nasopharynx. The disruption of the skeletal stability, with its associated effect on the soft tissue of the pharynx, may contribute to obstruction during negative pressure inspiration.4 Nasal fractures may also cause nasopharyngeal obstruction. The hemorrhage associated with a nasal fracture may be sufficient to result in airway irritability and aspiration of blood.
Le Fort II and III fractures, along with naso-orbital-ethmoidal (NOE) fractures, may involve a fracture of the cribriform plate of the ethmoid bone or the medial wall of the orbit. The fracture of these bones creates the risk for the endotracheal tube to enter the cranium or orbit with nasal intubation. This is a relative contraindication to nasotracheal intubation until a cranial base fracture has been ruled out. There is also a potential risk for bacteria or air to be forced into the cranial cavity with positive-pressure ventilation.5
Cervical Spine Injury
Cervical spine injury must be suspected in any patient with a maxillofacial injury. The incidence of cervical injury in the presence of facial fractures has been reported to be 1% to 6%.6–8 The higher percentage is among patients who were involved in a motor vehicle accident (MVA). The increased incidence probably is secondary to the forces sustained in the MVA and the associated hyperextension, hyperflexion, compression, and rotation of the cervical spine.9 However, no definitive relationship has been found between the mechanism of injury and a specific maxillofacial or cervical spine injury.
In the conscious patient, cervical spine injury is unlikely if the patient subjectively is without pain or paresthesia and objectively is without deformity or tenderness to palpation in a neutral position and during flexion and extension.10 If there is any positive finding, or if the patient is obtunded or not fully alert and able to concentrate, further investigation is warranted. The pediatric patient may be unable to provide reliable information and a lower threshold for further investigation is warranted. In the unconscious patient, flaccid areflexia, loss of rectal sphincter tone, diaphragmatic breathing, and bradycardia are suggestive of a cervical spine injury.
If further investigation is required, the diagnosis of a cervical injury is made radiographically. The examination must be able to detect fractures and ligamentous injuries. The examination must visualize all seven cervical vertebrae and the first thoracic vertebrae to be able to rule out a cervical injury. Fractures of the cervical spine are more reliably detected with a computed tomography (CT) scan compared with plain films (90% versus 58%), but ligamentous injuries are more reliably detected with plain films compared with CT scans (93% versus 54%).11 Immobilization of the neck in a neutral position is required until a definitive diagnosis is established, with the understanding that the urgency of the resuscitation may preclude the ability to obtain a definitive diagnosis for several hours to days. The best method of immobilization is achieved with a combination of a rigid cervical collar, a cervical-head immobilizer, and a backboard.12 Rigid cervical collars by themselves limit rotation and lateral movement to only 50% of normal and flexion and extension to only 30% of normal and do not provide adequate stabilization. An anesthetized or paralyzed patient should not remain on a backboard for a period exceeding 1 hour because of the risk for decubitus ulcers.
Cervical Airway Injury
Injuries to the cervical airway may result from blunt or penetrating trauma. The incidence of these injuries is low. Blunt trauma to the airway from a direct blow to the cervical airway or from severe flexion-extension injuries may result in a thyroid, cricoid, or laryngeal cartilage fracture, or laryngotracheal separation.13 A fracture of the thyroid cartilage is frequently associated with edema. Stridor, dyspnea, dysphagia, odynophagia, or gurgling may be suggestive of swelling of the airway. A muffled voice, hoarseness, or inability to speak may also be suggestive of a laryngeal fracture. A fracture of the cricoid cartilage is less common. It is frequently associated with an injury to the recurrent laryngeal nerve. Injury to this nerve results in vocal cord paralysis. Vocal cord paralysis impairs the ability to protect the airway, which can lead to pulmonary aspiration. Although the incidence of a cricoid cartilage fracture is rarer, there is a mortality of 43% associated with this injury compared with 11% seen with a thyroid fracture.14,15 Up to 70% of patients sustaining blunt airway trauma have a concurrent cervical spine injury.16
Thermal and Inhalation Injury
When the patient presents with a risk of thermal or inhalation injury, the examination must include looking for signs such as facial burns, singed facial hair, and/or carbonaceous debris in the nasal or oral secretions. These may be the only indications of potential respiratory problems because some patients may not demonstrate respiratory dysfunction on initial presentation. However, approximately 15% to 30% of burn patients develop some degree of respiratory dysfunction.17,18 Other early physical findings include wheezing, cough, dysphonia, and hoarseness. Upper airway edema, which may appear unremarkable initially, is an early contributing factor to respiratory distress. Within 2 hours, it may become notable, progressively worsening and necessitating intubation within 4 to 8 hours.19 The pediatric patient’s airway, with its relatively smaller diameter, is more susceptible to airway obstruction because any edema will have a more profound effect on airway patency. Late complications, such as parenchymal lung damage, may take several days to develop.
Carbon monoxide and cyanide are products of combustion; both cause tissue hypoxia. Hypoxia secondary to carbon monoxide toxicity occurs because carbon monoxide has a 250 times greater affinity for hemoglobin compared with oxygen. This displaces oxygen from its hemoglobin binding site and results in a lower oxygen-carrying capacity and lower blood oxygen content. The oxyhemoglobin dissociation curve is also shifted to the left. The leftward shift of the oxyhemoglobin dissociation curve results in less oxygen being released to the peripheral tissue.20
Monitoring oxygen saturation by pulse oximetry is inaccurate because these devices do not differentiate between oxyhemoglobin and carboxyhemoglobin.21,22 Serum carboxyhemoglobin levels should be obtained to establish the actual level of carbon monoxide present. Carboxyhemoglobin levels less than 20% cause headache and possible confusion. Carboxyhemoglobin levels between 20% and 40% present symptoms that include nausea, vomiting, disorientation, and visual impairment. Levels between 40% and 60% result in agitation, hallucinations, and coma, whereas levels greater than 60% are fatal.23 The half-life of carboxyhemoglobin is 4 hours. Oxygen therapy is indicated. The administration of 100% oxygen can shorten the half-life of carboxyhemoglobin to less than 1 hour. Hyperbaric oxygen (HBO) therapy has been recommended for carboxyhemoglobin levels of 30% or higher.24 Patients with neurologic symptoms should be considered for HBO regardless of their carboxyhemoglobin level.
Cyanide interferes with mitochondrial cytochrome function, resulting in tissue hypoxia. Nonspecific neurologic findings, including agitation and coma, are seen with cyanide toxicity. Lactic acidosis is also found with cyanide toxicity because it occurs with carbon monoxide toxicity. However, elevated levels in the patient without a significant burn injury and with ventilatory correction are more suggestive of cyanide toxicity.25 The mixed venous partial pressure of oxygen is also elevated in these patients. Cardiac rhythm disturbances are also not uncommon in these patients. Cyanide levels above 0.2 mg/liter are toxic and above 1 mg/liter are fatal.26